<?xml version="1.0" encoding="UTF-8"?><xml><records><record><source-app name="Biblio" version="7.x">Drupal-Biblio</source-app><ref-type>17</ref-type><contributors><authors><author><style face="normal" font="default" size="100%">Rena Normasari</style></author><author><style face="normal" font="default" size="100%">Bambang Purwanto</style></author><author><style face="normal" font="default" size="100%">Damayanti Tinduh</style></author></authors></contributors><titles><title><style face="normal" font="default" size="100%">Protective Effects of Rutinoside on Oxidative Induced Articular Cartilage Damage and Catabolic Activity in Rat Chondrocyte</style></title><secondary-title><style face="normal" font="default" size="100%">Pharmacognosy Journal</style></secondary-title></titles><keywords><keyword><style  face="normal" font="default" size="100%">Inflammation</style></keyword><keyword><style  face="normal" font="default" size="100%">Osteoarthritis</style></keyword><keyword><style  face="normal" font="default" size="100%">Oxidative stress</style></keyword><keyword><style  face="normal" font="default" size="100%">Rutinoside</style></keyword></keywords><dates><year><style  face="normal" font="default" size="100%">2024</style></year><pub-dates><date><style  face="normal" font="default" size="100%">April 2024</style></date></pub-dates></dates><volume><style face="normal" font="default" size="100%">16</style></volume><pages><style face="normal" font="default" size="100%">360-365</style></pages><language><style face="normal" font="default" size="100%">eng</style></language><abstract><style face="normal" font="default" size="100%">&lt;p class=&quot;rtejustify&quot;&gt;&lt;strong&gt;Objective:&lt;/strong&gt; This study aimed to look into the therapeutic potential of rutinoside in reducing articular cartilage degeneration in a rat model of osteoarthritis generated by monosodium iodoacetate (MIA). &lt;strong&gt;Methods:&lt;/strong&gt; We formed three groups of male Wistar rats: the OA, rutinoside, and control groups. Monosodium iodoacetate (3.0 mg) was injected intra-articularly into the knee joint to cause osteoarthritis. For four weeks, oral administration of rutinoside at 100 mg/kg/day was given to the groups that were given the treatment. Histological examination, immunohistochemistry, and biochemical tests were used to assess the level of articular cartilage injury, oxidative damage, catabolic activity, and biomarker expression. &lt;strong&gt;Results:&lt;/strong&gt; The results showed that treatments with rutinoside significantly reduced the damage to articular cartilage in rats with MIA-induced osteoarthritis. Compared to the osteoarthritis group, the rutinoside-treated groups showed enhanced cartilage structure, proteoglycan content, and chondrocyte organization. Immunohistochemistry revealed reduced NFκB, IL-1β, and MMP-13 expressions in the rutinosidetreated groups, indicating suppressed inflammatory and catabolic activity in chondrocytes. Additionally, rutinoside treatment increased SOD activity and decreased MDA levels, which showed less oxidative damage to the joint. A substantial drop in CTX-II levels was found by biochemical research, indicating less type II collagen breakdown. &lt;strong&gt;Conclusion: &lt;/strong&gt;According to a study, rutinoside effectively reduces oxidative damage and catabolic activity in chondrocytes, which can lead to decreased articular cartilage loss in a rat model of MIA-induced osteoarthritis. The study also found that rutinoside can control critical biomarkers such as NFκB, IL-1β, SOD, MDA, MMP-13, and CTX-II, highlighting its potential as a treatment for osteoarthritis. These findings provide valuable insights into using natural chemicals as a promising treatment for OA and suggest that rutinoside could potentially modulate the critical interplay between oxidative stress, inflammation, and chondrocyte catabolism in osteoarthritis. However, further research is required to understand the underlying molecular mechanisms and evaluate rutinoside's translational potential for OA therapy.&lt;/p&gt;
</style></abstract><issue><style face="normal" font="default" size="100%">2</style></issue><work-type><style face="normal" font="default" size="100%">Research Article</style></work-type><section><style face="normal" font="default" size="100%">360</style></section><auth-address><style face="normal" font="default" size="100%">&lt;p&gt;&lt;strong&gt;Rena Normasari&lt;sup&gt;1,2&lt;/sup&gt;, Bambang Purwanto&lt;sup&gt;3*&lt;/sup&gt;, Damayanti Tinduh&lt;sup&gt;4&lt;/sup&gt;&lt;/strong&gt;&lt;/p&gt;

&lt;p&gt;&lt;sup&gt;1&lt;/sup&gt;Doctoral Program, Faculty of Medicine, Airlangga University, INDONESIA.&lt;/p&gt;

&lt;p&gt;&lt;sup&gt;2&lt;/sup&gt;Pathology Anatomy Department, Medical Faculty, Jember University, INDONESIA.&lt;/p&gt;

&lt;p&gt;&lt;sup&gt;3&lt;/sup&gt;Physiology Department, Faculty of Medicine, Airlangga University, INDONESIA. 4Physical Medicine and Rehabilitation Department, Faculty of Medicine, Airlangga University, INDONESIA.&lt;/p&gt;
</style></auth-address></record><record><source-app name="Biblio" version="7.x">Drupal-Biblio</source-app><ref-type>17</ref-type><contributors><authors><author><style face="normal" font="default" size="100%">Rena Normasari</style></author><author><style face="normal" font="default" size="100%">Bambang Purwanto</style></author><author><style face="normal" font="default" size="100%">Damayanti Tinduh</style></author></authors></contributors><titles><title><style face="normal" font="default" size="100%">A Comparative Study of CFA and MIA Induction Models in Rat  Knee Arthritis</style></title><secondary-title><style face="normal" font="default" size="100%">Pharmacognosy Journal</style></secondary-title></titles><keywords><keyword><style  face="normal" font="default" size="100%">CFA</style></keyword><keyword><style  face="normal" font="default" size="100%">CTX-II</style></keyword><keyword><style  face="normal" font="default" size="100%">IL-1β</style></keyword><keyword><style  face="normal" font="default" size="100%">MIA</style></keyword><keyword><style  face="normal" font="default" size="100%">Osteoarthritis</style></keyword></keywords><dates><year><style  face="normal" font="default" size="100%">2023</style></year><pub-dates><date><style  face="normal" font="default" size="100%">December 2023</style></date></pub-dates></dates><volume><style face="normal" font="default" size="100%">15</style></volume><pages><style face="normal" font="default" size="100%">1197-1201</style></pages><language><style face="normal" font="default" size="100%">eng</style></language><abstract><style face="normal" font="default" size="100%">&lt;p class=&quot;rtejustify&quot;&gt;This study presents another comparative review of knee joint arthritis induction in rats using two distinct methods: Complete Freund's Adjuvant (CFA) and monosodium iodoacetate (MIA). Different variables are assessed, including bodyweight changes, knee bend scores, and knee diameter measurements, as well as the quantification of interleukin-1β (IL-1β) and C-telopeptide of type II collagen (CTX-II) levels. CFA or MIA induction was used on rats, and 14 days were observed. Our data show that the impact of arthritis induction varies significantly across the two models. Both the CFA and MIA groups showed different changes in terms of bodyweight changes, knee bend scores, and knee diameter variations. Furthermore, the levels of IL-1β and CTX-II, both known indicators of inflammation and cartilage degeneration, were measured. Notably, IL-1β levels in the CFA group were considerably higher than in the MIA-induced rats, although CTX-II concentrations showed a contrary pattern. These findings highlight the need to carefully consider the induction approach when performing arthritis investigations in rats since the model used has a major impact on the reported physiological alterations. This study's comparative analysis provides useful information for researchers looking to use rat knee joint arthritis models, laying the groundwork for a better-informed selection of the best induction strategy depending on desired outcome metrics.&lt;/p&gt;
</style></abstract><issue><style face="normal" font="default" size="100%">6</style></issue><work-type><style face="normal" font="default" size="100%">Research Article</style></work-type><section><style face="normal" font="default" size="100%">1197</style></section><auth-address><style face="normal" font="default" size="100%">&lt;p class=&quot;rtejustify&quot;&gt;&lt;strong&gt;Rena Normasari&lt;sup&gt;1&lt;/sup&gt; , Bambang Purwanto&lt;sup&gt;2,&lt;/sup&gt;*, Damayanti Tinduh&lt;sup&gt;3&lt;/sup&gt;&lt;/strong&gt;&lt;/p&gt;

&lt;p&gt;&lt;sup&gt;1&lt;/sup&gt;Doctoral Program, Medical Faculty, Airlangga University, Surabaya, INDONESIA.&lt;/p&gt;

&lt;p&gt;&lt;sup&gt;2&lt;/sup&gt;Physiology Department, Medical Faculty, Airlangga University, Surabaya, INDONESIA.&lt;/p&gt;

&lt;p&gt;&lt;sup&gt;3&lt;/sup&gt;Physical Medicine and Rehabilitation Department, Medical Faculty, Airlangga University, Surabaya, INDONESIA.&lt;/p&gt;
</style></auth-address></record></records></xml>